The induction of cleft palates in A/J mice in response to the administration of a glucocorticoid offers an unusual laboratory model for studies on birth defects. Our hypothesis is that the genome is involved, and experiments are proposed to assay for various aspects of the genomic structure and function. The basic question is whether, in response to the administration of triamcinolone acetonide (TAC), the gene is modified. The methods call for the isolation of nuclei and cytosol from maxillary processes both from the normal and TAC-injected A/J mouse embryos, for the qualitative analysis on soluble cytoplasmic proteins, for the isolation and characterization of HnRNA, and for the incubation of nuclei in vitro for studies on transcription. Chromatin will also be isolated from nuclei and will be fractionated for the isolation and identification of TAC-binding proteins, which form a part of the nonhistone chromosomal proteins. The assays on the complexity of HnRNA both from normal and TAC-injected A/J mouse embryos will include hybridization of DNA complimentary to normal HnRNA. Various methods are proposed to increase the sensitivity of the method of hybridization to detect as little as 10 to the negative 6th power - 10 to the negative 5th poser of the transcripts in the RNA population. By such methods we may be able to detect differences in HnRNA population occurring in response to TAC ad in comparison to untreated A/J mouse embryos. This data will be analyzed also relative to observed changes in the cytoplasmic proteins, the gene end products.